Journal
PPAR RESEARCH
Volume 2022, Issue -, Pages -Publisher
HINDAWI LTD
DOI: 10.1155/2022/8161946
Keywords
-
Categories
Funding
- National Natural Science Foundation of China
- Yangfan Plan of Shanghai Science and Technology Commission
- [82100638]
- [82102956]
- [82002539]
- [20YF1443300]
- [21YF1435400]
Ask authors/readers for more resources
Luteolin preconditioning can reduce hepatocyte injury caused by hepatic ischemia-reperfusion and exert its effects by suppressing inflammation, apoptosis, and autophagy. In addition, luteolin can inhibit ERK phosphorylation and activate PPARα.
Hepatic ischemia-reperfusion (IR) injury is a clinically significant process that frequently occurs in liver transplantation, partial hepatectomy, and hemorrhagic shock. The aim of this study was to explore the effectiveness of luteolin in hepatic IR injury and the underlying mechanism. BALB/c mice were randomly divided into six groups, including normal controls (NC), luteolin (50 mg/kg), sham procedure, IR+25 mg/kg luteolin, and IR+50 mg/kg luteolin group. Serum and tissue samples were collected at 6 and 24 h after reperfusion to assay liver enzymes, inflammatory factors, expression of proteins associated with apoptosis and autophagy, and factors associated with the extracellular signal-regulated kinase/peroxisome proliferator-activated receptor alpha (ERK/PPAR alpha) pathway. Luteolin preconditioning decreased hepatocyte injury caused by ischemia-reperfusion, downregulated inflammatory factors, and inhibited apoptosis and autophagy. Luteolin also inhibited ERK phosphorylation and activated PPAR alpha.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available